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Updated: May 9, 2026
11:29
miRNA Expression Analyses in Prostate Cancer Clinical Tissues
Published on: September 8, 2015
Dysregulated methylation at imprinted genes in prostate tumor tissue detected by methylation microarray
Daniel I Jacobs1, Yingying Mao, Alan Fu
1Yale School of Public Health, Yale University School of Medicine, New Haven, CT, USA.
BMC Urology
|July 30, 2013
Summary
Prostate cancer shows widespread disruption of gene imprinting, with significant methylation changes in numerous genes. This epigenetic dysregulation, particularly in tumor suppressor genes, indicates a broader impact than previously understood.
Area of Science:
- Epigenetics
- Cancer Biology
- Genomics
Background:
- Imprinting is a critical epigenetic mechanism regulating gene expression, frequently altered in cancer.
- Previous studies identified loss of imprinting (LOI) in only two genes (IGF2, TFPI2) in prostate cancer.
- Systematic investigation of methylation changes across all imprinted gene regions in prostate cancer was lacking.
Purpose of the Study:
- To comprehensively analyze methylation patterns across imprinted gene regions in prostate cancer.
- To identify specific imprinted genes exhibiting altered methylation and potential loss of imprinting (LOI) in tumors compared to normal tissue.
- To correlate methylation changes with gene expression to understand the functional impact of imprinting dysregulation.
Main Methods:
- Utilized Illumina Infinium Methylation Assay to assess methylation at 396 CpG sites in 56 promoter regions from 12 prostate tumor/normal tissue pairs.
- Validated candidate loss of imprinting (LOI) events using Sequenom EpiTYPER assay on individual samples.
- Confirmed findings with gene expression data from public datasets.
Main Results:
- Observed significant methylation increases at 52 sites and decreases at 17 sites across 28 unique genes (P < 0.05).
- Strongest evidence for loss of imprinting (LOI) was found in tumor suppressor genes: DLK1, PLAGL1, SLC22A18, TP73, and WT1.
- Differential gene expression patterns in tumors were consistent with LOI, and WT1 hypermethylation was quantitatively confirmed.
Conclusions:
- Prostate cancer exhibits more extensive genetic imprinting dysregulation than previously recognized.
- The identified widespread epigenetic alterations warrant further investigation into their role in prostate cancer development and progression.
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